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anti-Human Aquaporin 4 Antikörper:
anti-Mouse (Murine) Aquaporin 4 Antikörper:
anti-Rat (Rattus) Aquaporin 4 Antikörper:
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Human Polyclonal Aquaporin 4 Primary Antibody für IF (p), IHC (p) - ABIN671181
Duan, Hao, Fan, Wang, Liu, Hao, Xu, Liu, Zhang: The role of neuropeptide Y and aquaporin 4 in the pathogenesis of intestinal dysfunction caused by traumatic brain injury. in The Journal of surgical research 2013
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Human Monoclonal Aquaporin 4 Primary Antibody für IHC (fro), IHC (p) - ABIN2477485
Endert, Ritter, Schumann: [Isotope methods in the radiological diagnosis of venous disease. II. Indications and accuracy (author's transl)]. in RöFo : Fortschritte auf dem Gebiete der Röntgenstrahlen und der Nuklearmedizin 1980
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Human Polyclonal Aquaporin 4 Primary Antibody für ICC, IF - ABIN4281307
Lopez-Rodriguez, Acaz-Fonseca, Viveros, Garcia-Segura: Changes in cannabinoid receptors, aquaporin 4 and vimentin expression after traumatic brain injury in adolescent male mice. Association with edema and neurological deficit. in PLoS ONE 2015
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Human Monoclonal Aquaporin 4 Primary Antibody für EIA, IHC (fro) - ABIN119570
Bódis, Nagy, Németh, Mózsik: Active water selective channels in the stomach: investigation of aquaporins after ethanol and capsaicin treatment in rats. in Journal of physiology, Paris 2001
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Human Monoclonal Aquaporin 4 Primary Antibody für EIA, IHC (fro) - ABIN119571
Esposito, Imitola, Lu, De Filippis, Scuderi, Ganesh, Folkerth, Hecht, Shin, Iuvone, Chesnut, Steardo, Sheen: Genomic and functional profiling of human Down syndrome neural progenitors implicates S100B and aquaporin 4 in cell injury. in Human molecular genetics 2008
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Ordered disorder of the astrocytic dystrophin (zeige DMD Antikörper)-associated protein complex in the norm and pathology.
the AQP4 could play a role in the regulation of water balance and ion transport in the sensory cells of zebrafish, bringing new data for the utilizing of this experimental model in the biology of sensory system.
These results suggest that AQP4 is damaged first and decrease of EAAT-2 (zeige SLC1A2 Antikörper) may follow in pathogenesis of cortical degeneration. This is the first demonstration of decrease of AQP4 and its association with EAAT-2 (zeige SLC1A2 Antikörper) decrease in AIDS brain, suggesting a role in the pathogenesis of HIV-associated neurocognitive disorders.
The purpose of this study was to determine whether or not aquaporin-4 (AQP4) gene mutations are related to the pathogenesis of inflammatory demyelinating diseases in the central nervous system.
Comparative molecular dynamics study of neuromyelitis optica-immunoglobulin G binding to AQP4 extracellular domains has been presented.
Osmotic water permeabilities of aquaporins AQP4, AQP5 (zeige AQP5 Antikörper), and GlpF from near-equilibrium simulations have been presented.
A clear correlation between AQP4 expression and ADCmax values in grade I meningioma was identified.
Peritumoral brain edema in patients with meningiomas may depend on AQP4 expression grades and not on tumor grade, tumor volume, Ki-67 (zeige MKI67 Antikörper) expression, and cell count.
AQP4 antibodies were higher in neuromyelitis optica Chinese Han patients with circulating auto-antibodies.
Retinal nerve fiber layer may be better preserved in MOG-IgG versus AQP4-IgG optic neuritis.
AQP4-autoantibody serostatus correlated with poor visual outcome in neuromyelitis optica (Meta-analysis)
Data show that aquaporin-4 (AQP4) and myelin-oligodendrocyte glycoprotein (MOG) autoantibodies double positive neuromyelitis optica spectrum disorder (NMOSD) patients had a multiphase disease course with a high annual relapse rate.
In this study, altered AQP4 expression was associated with aging brains.
Aquaporin-4 has two isoforms, M1 and M23, whose transcripts are driven by distinct promoters. A fragment located between exons 0 and 1 of the aquaporin-4 gene, which had been thought to be the promoter for M23, lacked enhancers functioning in astrocytes. When the astrocyte-specific enhancer (ASE (zeige ARSE Antikörper)) of the M1 promoter is connected to the putative M23 core promoter, it also works in astrocytes.
In anhedonic mice, the expression of the water channel aquaporin 4 (AQP4), a factor in glymphatic pathway dysfunction, was down-regulated in cortex and hippocampus.
The results of this study that AQP4 and GLT1 do not have a strong physical interaction between them and are, instead, differentially regulated.
Study suggests that astaxanthin may exert neuroprotection following traumatic brain injury by ameliorating AQP4/NKCC1 (zeige SLC12A2 Antikörper)-mediated cerebral edema, and NKCC1 (zeige SLC12A2 Antikörper) inactivation inhibitions the upregulation of AQP4 after traumatic brain injury.
this study identified and fine mapped the major T-cell epitope of AQP4 and observed that in a transfer model, AQP4-specific T cells alone induced an encephalomyelitic syndrome, however, only in the additional presence of anti-AQP4 antibodies, central nervous system lesions are reminiscent of neuromyelitis optica
Study found that aquaporin-4 deficiency facilitated fear memory extinction and NMDA receptors-dependent long-term depression in the CA3 (zeige CA3 Antikörper)-CA1 (zeige CA1 Antikörper) hippocampal pathway.
Study demonstrated evidence of beta-dystroglycan cleavage by matrix metalloproteinase-2 (zeige MMP2 Antikörper)/-9 in permanent middle cerebral artery occlusion mouse brains; this cleavage was implicated in aquaporin-4 redistribution and brain edema in cerebral ischemia.
This study demonstrated that AQP4 dorsal hippocampal protein expression was significantly downregulated at 1day post epilepsy and was followed by a gradual return to baseline levels with a significant increase in ipsilateral protein levels by 30days post epilepsy.
The major findings in this study were (1) a higher AQP4 immunogold labeling density over parenchymal astrocytic membranes in human subjects than in mice, and (2) a lower degree of AQP4 immunogold polarization to perivascular astrocytic endfoot membranes in humans compared with mice. In the human individuals, endfoot AQP4 polarization did not differ between capillary and arteriolar vessel segments.
TRPV4 (zeige TRPV4 Antikörper)-AQP4 interactions 'turbocharge' astroglial sensitivity to small osmotic gradients
AQP4 plays an important role in mediating brain edema in hypoxic-ischemic encephalopathy.
constitutive recycling of AQP2 (zeige AQP2 Antikörper) does not require phosphorylation at any C-terminal sites
In conclusion, HPO (zeige GFER Antikörper) can decrease AQP4 expression in brain tissue of rabbits with cerebral hemorrhage to suppress the progression of brain edema and promote repairing of injured tissue.
AQP4 may play an important role in brain edema after severe scald (zeige RDH11 Antikörper).
In the guinea pig AQP4 is localised to enteric glial cells.
This gene encodes a member of the aquaporin family of intrinsic membrane proteins that function as water-selective channels in the plasma membranes of many cells. The encoded protein is the predominant aquaporin found in brain. Two alternatively spliced transcript variants encoding distinct isoforms have been found for this gene.
, aquaporin 4
, aquaporin type4
, mercurial-insensitive water channel
, aquaporin 4.M23
, mercurial insensitive water channel
, water channel